The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao 266003, China.
The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao 266003, China.
Environ Toxicol Pharmacol. 2022 Jul;93:103867. doi: 10.1016/j.etap.2022.103867. Epub 2022 Apr 25.
As a common pollutant in marine environment, benzo[a]pyrene (B[a]P) has high toxicity to economic shellfish. In order to explore the mechanism of oxidative stress and apoptosis, the effects of 0, 2, 4, 8 μg/mL B[a]P on gill cells of C. farreri at 12 and 24 h were studied. The results showed that B[a]P decreased the activity of gill cells, increased the content of reactive oxygen species (ROS) and the expression of antioxidant defense genes. Besides, B[a]P could induce oxidative damage to nucleus and mitochondria. The gene expression and enzyme activity of apoptosis pathway related factors were changed. In conclusion, these results showed that B[a]P could cause oxidative stress and oxidative damage in gill cells of C. farreri, and mediate gill cell apoptosis through mitochondrial pathway and death receptor pathway. This article provides a theoretical basis for clarifying the molecular mechanism of PAHs-included oxidative stress and apoptosis in bivalves.
作为海洋环境中的一种常见污染物，苯并[a]芘（B[a]P）对经济贝类具有高毒性。为了探讨氧化应激和细胞凋亡的机制，研究了 0、2、4、8μg/mL B[a]P 对栉孔扇贝（C. farreri）鳃细胞在 12 和 24 h 的影响。结果表明，B[a]P 降低了鳃细胞的活性，增加了活性氧（ROS）的含量和抗氧化防御基因的表达。此外，B[a]P 还可诱导细胞核和线粒体发生氧化损伤。凋亡途径相关因子的基因表达和酶活性发生变化。总之，这些结果表明 B[a]P 可引起栉孔扇贝鳃细胞发生氧化应激和氧化损伤，并通过线粒体途径和死亡受体途径介导鳃细胞凋亡。本文为阐明多环芳烃诱导的贝类氧化应激和凋亡的分子机制提供了理论依据。
